cornea

1. cornea Švehlíková G. Department ofOphthalmology LF UPJS v Košiciach Prednosta: prof. MUDr. Juhás T., DrSc.

2. Anatomyofthecornea • Epitelium • Stroma • Endotelium

3. Clinicalevaluation

4. SLIT-LAMP BIOMICROSCOPY

5. Fluorescein staining of the cornea

6. Cornea Keratometry - measuring the curvature of the anterior surface of the cornea, particularly for assessing the extent and axis of astigmatism Corneal Topography Map

7. Cornea keratoscopy Normal cornea keratoconus Pachymetry - corneal thickness

8. Specularmicroscope Normal endothelial cells Pathologic endothelium

9. Developmentalanomalies

10. Microcornea • rare, hereditary, • horizontalcorneal diameter is 10 mm or less • otherwisenormalstructure • otherocularabnorm. – glaucoma, cataract, iris abnorm...

11. Megalocornea • rare, bilat. • corneal diameter is 13 mm or more • structure is normal • high myopia, astigmatism

12. Degenerativechangesofthecornea Occur with age or secondary to exogenous noxious agents Often more pronounced in one eye

13. Arcuslipoides - senilis • yellow-whitecircularopacity in theperipheralcornea • consistoflipidsdeposited in thecornealstroma • highprevalence – arcussenilis

14. Bandkeratopathy • deposition of calcium salts in the subepitelial space • causes - chronic iridocyclitis, phtisis bulbi, metabolic – increased serum calcium , chronic renal failure • Treatment: - repeated application of calcium binding agent EDTA (ethylenediaminetetraacetic acid) - Excimer laser phototherapeutic keratectomy has been effectively performed to treat more extensive cases

15. Spheroiddegeneration • yellow subepitelial and stromal deposits • visual impairment, severe fotofobia, pain • frequent exposure to sunlight

16. Salzmann´snodulardereneration • multiple bluish-white superficial nodules • occurs secondary to chronic keratitis and trauma

17. Cornealdystrophies Progresive, usualy bilateral, genetically determined disorders Age of presentation – 1. – 4. decade

18. Cornealdystrophies • Classification • 1. anteriorD. – Cogan microcystic D, Reis- Bucklers D, Meesman D, Schnyder D • 2. stromal D. – latice D, granular D, macular D • 3. posterior D. – Fuchs endotelial, posterior polymorphousD

19. Coganmicrocysticdystrophy • map-dot-fingerprint D • four types of lesion are seen either in isolation or in combination : dots, microcysts, map-like, fingerprint-like • often asymptomatic • 10% recurent cornela erosions

20. Meesmanndystrophy • AD • rare, • multiple intraepithelial cysts across the entire cornea • symptoms – foreign body sensation, photophobia • usually no th

21. Latticedystrophy • AD • subepitelial and intrastromal branching lattice figures • accumulation of amyloid material • complication – recurent epitelial breaks

22. Granulardystrophy • AD • multiple grey-white, snowflake-like, sharply demarcated opacites • beginning in the epithelium, later in the entire stroma • histology – hyaline deposits

23. Maculardystrophy • systemic disorder of keratan sulfate metabolism • AR • progresive, greyish opacification

24. Fuchsendotelialdystrophy • slowly progresive disease • Signs: • Asymmetrical, bilateral, presents in the fifth or sixth decade • bilateral primary cornea guttata and a reduced endothelial cell density • advanced stage: • endothelial cell pump decompensation results in corneal edema • bullous keratopathy • histology shows a thickened Descemet’s membrane and endothelial cell loss.

25. Image obtainedby specular microscopyshows destruction ofthe endothelialcells (right side ofimage). In comparison,the leftside andthe middle (magnifiedview) ofthe image showan intact endotheliumwith aclearly visible honeycombstructure

26. KERATOCONUS degenerative, non-inflammatory disorder of the cornea number of patients affected varies between 1 in 3,000 and 1 in 10,000 depending on geographic location asymetrical progresive thinning manifestation between the age of 10-20 the causes of keratoconus are poorly understood - increased activity of proteinase enzymes and a reduced activity in the proteinase enzyme inhibitors. This imbalance can destroy the structural proteins and supporting substrates within the cornea, resulting in thinning and loss of the normal mechanical strength.

27. Early signs irregular astigmatism slit-lamp examination: - Vogt lines - very fine, vertical lines in the cornea - Fleishers ring - yellow-brown ring of iron pigment seen at the base of the cone beneath the epithelium corneal topography is the most sensitive method for detecting very early keratoconus by identifying subtle, inferior corneal steepening

28. Late signs progressive corneal thinning, with poor vision from marked irregular astigmatism the apex of the cone is the thinnest area and is usually displaced inferiorly just below the centre corneal protrusion causing bulging of the lower lid on looking down (Munson sign).

29. Acute Hydrops in advanced cases, spontaneous ruptures of the Descemet's membrane can occur, causing a tear near the apex of the cone the rupture allows aqueous to pass into the cornea resulting in significant corneal oedema and opacification although the break usually heals within 6-10 weeks and the corneal oedema clears, a variable amount of corneal scarring may develop corneas that do not recover transparency may require a corneal transplant

30. Treatment • depends of the degree of ectasia • early and mild cases can be treated with astigmatic spectacle correction and soft toric contact lenses • as the disease progresses - rigid contact lenses • 10-25% of patients with keratoconus progress – surgical intervention • Surgical options include: • 1. Corneal Collagen Cross-linking with Riboflavin • 2. Corneal transplantation • 3. Intra-corneal ring segment insert

31. Corneal Collagen Cross-linking with Riboflavin • new treatment modality, • stabilize the process • the aims of the treatment are to increase the mechanical stability of the cornea by inducing cross linkage between the corneal collagen fibres • under topical anaesthesia • as riboflavin does not penetrate the corneal epithelium this is removed and riboflavin (vitamin B2) is applied as a photosensitiser • the tissue is then exposed to UVA (370nm) light for about 30 minutes • this allows the generation of additional connections, so-called cross-linkings, between the individual collagen fibres of the cornea.

32. Corneal transplantation • Corneal transplantation (grafting) replaces the central 7-8 millimeters of the cornea with a donor cornea that has been prepared by an eye bank 

33. Corneal transplantation • different types: • Penetrating Keratoplasty • Lamellar Keratoplasty • Decemet’s Stripping with Endothelial Keratoplasty (DSEK)

34. Cornealtransplantation Penetrating Keratoplasty Lamellar Keratoplasty Decemet’sStrippingwithEndothelialKeratoplasty (DSEK)

35. Indications • to improve vision • to reduce pain • or to maintain the structural integrity of the eye Disorders: - Bullous keratopathy (pseudophakic or aphakic, Fuchs' endothelial dystrophy) - Keratoconus - Keratitis or postkeratitis (caused by viral, bacterial, fungal, or Acanthamoeba infection or perforation) - Corneal stromal dystrophies

36. PenetratingKeratoplasty ( PK) • full thickness corneal transplantation, PK is the commonest type of corneal graft • the sutures are normally removed 1 to 2 years after surgery

37. PK

38. PK

39. PK Interrupted sutures Single runningsuture Suturing techniques Doublerunningsuture Stp. PK

40. LamellarKeratoplasty • in DLK a central disc of tissue including the front 95% of the cornea is replaced with a transplant tissue • importantly, the endothelial cell layer is left in place • performed as an alternative to PK in keratoconus, because this cell layer remains healthy in keratoconus

41. LAMELLAR KERATOPLASTY Advantages for DLK include: • fewer problems with rejection - the endothelial cell layer is the main target of immunological attack in corneal transplant rejection reactions, and damage to this layer during graft rejection can cause the graft to fail • leaving the original endothelial layer in place with a DLK avoids most rejection problems Disadvantages for DLK include • reduced visual clarity - some visual clarity is lost as a result of light scatter at the interface between the transplant and the host tissue in all partial thickness corneal grafting techniques • technical difficulty

42. Decemet’sStrippingwithEndothelialKeratoplasty (DSEK) • partial-thickness corneal transplant that replaces only the endothelial layer • instead of replacing the entire cornea the surgeon strips-away a delicate membrane along the backside of the cornea • thin piece of donor tissue containing the endothelial cell layer is inserted onto the back surface of the patient’s cornea • can be performed with topical anesthesia and small incisions • no stitching is required

43. DSEK • is appropriate for patients in which the endothelial cell layer is dysfunctional in cases of Fuchs’ dystrophy or post cataract surgery endothelial dysfunction (pseudophakic bullous keratopathy)Advantages of DSEK as compaired to standard corneal transplantation may include: • Better shape – problems with astigmatism are uncommon, visual recovery is faster • No suture problems - two of the commonest reasons for graft failure in PK are rejection and infection. Both problems may be precipitated by suture loosening or breakage. Because there are no sutures on the corneal surface after DSEK, these problems are avoided Disadvantages • technical difficulty

44. DSEK Only patients with endothelial cell problems are candidates for DSEK

45. Complications: • Graft rejection • Infection (intraocular and corneal) • Wound leak • Glaucoma • Graft failure • High refractive error (especially astigmatism, myopia, or both) • Recurrence of disease (with herpes simplex or hereditary corneal stromal dystrophy).

46. Cornealinfections Viruses Bacteria Fungi Protozoa

47. Epidemickeratoconjunctivitis Adenovirus Epidemic – highly infectious Inicial acute conjunctivitis, after 3 weeks – subepitelial opacities – spontaneously disappear

48. Herpes simplexinfection • DNA virus • infectionextremnlycommon, 90% ofthepopulation are seropositivefor HSV antibidies • most infection are subclinical • twotypes : HSV-1 ( face, lips, eyes) HSV-2 (genital) • HS virus

49. HSV1 LatentInfection • primaryinf. – subclinical or mildsymptoms • recurentinf. – thevirustravelsuptheaxonofsensory nerve to its ganglion, whereit lies in a latent state • in somepatientsthevirusreactivates, replicates and travelsdowntheaxon to itstargettissue, causingrecurrentlesion

50. Primaryocularinfection • Typicaly in children Blepharoconjunctivitis • benign, self-limited • skin lesioninvolvethelids and periorbitalarea • conjunctivitis – akute, waterydischarge, preauricularadenopathy. • Th : topicalantiviralointment 5x/day Keratitis • uncommon, fineepitelialpunctate • in somepatientsprogress